ABSTRACT
Objective:To report one case of diabetic ketoacidosis complicated by acute myocardial infarction and upper gastrointestinal bleeding, and make a certain summary to its diagnosis and treatment in order to improve the treatment of these critically ill patients.Methods:One patient was admitted to Guizhou Aerospace Hospital on November 14, 2021 due to fatigue and vomiting for 2 days, and worsened symptoms accompanied by poor consciousness for 1 day. The patient was diagnosed with diabetic ketoacidosis complicated by acute myocardial infarction and upper gastrointestinal bleeding. The clinical symptoms, signs, laboratory examinations, and follow-ups of the patient were analyzed systematically and retrospectively.Results:After volume state assessment using a combined way, the patient was treated with appropriate fluid replacement, hypoglycemic, antiplatelet, anticoagulant, and acid inhibition strategies. After treatment, ketoacidosis and upper gastrointestinal bleeding were corrected, blood glucose gradually stabilized, and myocardial necrosis markers troponin and N-terminal brain natriuretic peptide precursor became normal.Conclusion:Treatments of diabetic ketoacidosis, acute myocardial infarction, and upper gastrointestinal bleeding are contradictory. Therefore, analyzing this patient's diagnosis and treatment is of great significance for improving treatment and reducing the mortality of these critically ill patients.
ABSTRACT
Background: Inflammation has an essential role in atherosclerosis that is the leading reason for acute coronary syndrome (ACS) which includes acute myocardial infarction (AMI) and unstable angina (UA). The objective of this work was to study the existence of difference in Neutrophil to Lymphocyte ratio and its relation to inflammatory markers between cases with AMI and cases with chronic coronary syndrome. Methods: This work included sixty consecutive cases with AMI and ACS who presented to cardiovascular medicine department at Tanta university hospital. The cases were classified into two equal groups; group I: cases with AMI and group II: cases with chronic coronary syndrome. All participants were subjected to ECG, Echocardiography, color Doppler, coronary angiography and laboratory investigations as differential CBC, cardiac enzymes, troponine, CK, CK-MB, CRP, urea, creatinine and random blood sugar. Patients who didn’t meet the criteria for invasive treatment, continued on medication and further noninvasive investigations done, starting from stress ECG, stress echocardiography, or CCTA. Results: There were insignificantly different between the two groups regarding age, gender and residency (p= 1.00). There was insignificant difference between the two groups regarding hypertension (p= 0.592), DM (p= 0.795) and dyslipidemia (p= 0.504). 7 (23.3%) cases were smokers in group I and 8(26.7%) patients were smokers in group II with insignificantly different between the two groups (p= 1.00). Conclusions: NLR is a powerful marker of myocardial damage in acute myocardial cases.
ABSTRACT
Background: Arrhythmias commonly occur early in acute myocardial infarction and remain a common cause of sudden death in AMI. Magnesium has been implicated in the pathogenesis of acute myocardial infarction and its complication like arrhythmia. Magnesium improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death. It improves vascular tone, peripheral vascular resistance, after load and cardiac output and reduces cardiac arrhythmias. The objective of this study to investigate the serum magnesium level and QTc interval prolongation in AMI and its correlation with arrhythmias.Methods: In this study, 200 patients of AMI were enrolled. ECG and cardiac parameters were examined. Serum magnesium level is measured and the QTc interval was calculated.Results: MI was more prevalent in the male patients (63.3%) and age group of 41-50 years. Hypertension (35.7%), smoking (34.2%), and diabetes (23.1%) were the major risk factor for MI. Mean serum magnesium level was 1.64±0.37 among those having arrhythmia that is significantly low as compared to those having no arrhythmia among which mean serum magnesium level was 2.28±0.31 (p<0.001). Mean QTc was higher (546.88 ms vs. 404.33ms) in patients documented with arrhythmia compared with those who had no arrhythmia (p<0.001).Conclusions: In acute myocardial infarction, patients with low magnesium levels and prolonged QTc interval are more prone to get arrhythmias. So magnesium treatment can be considered in patients of acute myocardial infarction with low magnesium levels.
ABSTRACT
Objective:To evaluate the cardioprotective effect of Nigella sativa L.(N.sativa) in isoproterenol-induced myocardial infurction (MI).Methods:Groups were treated with different doses of ethanol extract of N.sativa (EENS)and N.sativa oil alone and along with enalapril for 28 days.MI was induced by subcutaneous administration of isoproterenol (85 mg/kg) in two consecutive doses.Levels of cardiac biomarkers and antioxidant enzymes such as creatine kinase-N-acetyl-L-cysteine,lactate dehydrogenase,aspartate aminotrmsferasc,malondialdehyde,supcroxide dismutase,reduced glutathione and catalase were evaluated along with gross histopathological examination.Results:lsoproterenol (85 mg/kg) induced MI by causing the significant (P ＜ 0.01)reduction in the activity of cardiac biomarkers (creatine kinase-N-acetyl-L-cysteine,lactate dehydrogenase,aspartate aminotransferase) and antioxidant markers (superoxide dismutase,catalase,glutathione) along with significant (P ＜ 0.01) increase in the level of malondialdehyde.Furthermore,histopathological evaluation also confirmed the isoproterenol-induced MI.Pretreatment with EENS (800 mg/kg) and combination of EENS (800 mg/kg) with enalapril (1 mg/kg) significantly (P ＜ 0.01) prevented the development of these alteration and restored activity of cardiac biomarkers as well as antioxidant markers almost near to normal levels.Histopathological evaluation of cardiac tissue further confirmed the restoration of biochemical activity,Conclusions:Experimental findings thus indicate that EENS (800 mg/kg) demonstrated cardioprotective effect against isoproterenol-induced MI by restoring cardiac biomarkers and antioxidant status.
ABSTRACT
Objective To evaluate the cardioprotective effect of Nigella sativa L. (N. sativa) in isoproterenol-induced myocardial infarction (MI). Methods Groups were treated with different doses of ethanol extract of N. sativa (EENS) and N. sativa oil alone and along with enalapril for 28 days. MI was induced by subcutaneous administration of isoproterenol (85 mg/kg) in two consecutive doses. Levels of cardiac biomarkers and antioxidant enzymes such as creatine kinase–N-acetyl-L-cysteine, lactate dehydrogenase, aspartate aminotransferase, malondialdehyde, superoxide dismutase, reduced glutathione and catalase were evaluated along with gross histopathological examination. Results Isoproterenol (85 mg/kg) induced MI by causing the significant (P < 0.01) reduction in the activity of cardiac biomarkers (creatine kinase–N-acetyl-L-cysteine, lactate dehydrogenase, aspartate aminotransferase) and antioxidant markers (superoxide dismutase, catalase, glutathione) along with significant (P < 0.01) increase in the level of malondialdehyde. Furthermore, histopathological evaluation also confirmed the isoproterenol-induced MI. Pretreatment with EENS (800 mg/kg) and combination of EENS (800 mg/kg) with enalapril (1 mg/kg) significantly (P < 0.01) prevented the development of these alteration and restored activity of cardiac biomarkers as well as antioxidant markers almost near to normal levels. Histopathological evaluation of cardiac tissue further confirmed the restoration of biochemical activity. Conclusions Experimental findings thus indicate that EENS (800 mg/kg) demonstrated cardioprotective effect against isoproterenol-induced MI by restoring cardiac biomarkers and antioxidant status.
ABSTRACT
Interruption of blood supply to heart results in acute myocardial infarction (AMI) and further leads to damaging of the heart muscles. Available drugs for the treatment MI have one or other side effects, and there is a need for development of better alternative drugs. Here comes the role of herbal sources. In this study, we evaluated cardioprotective effect of Cyperus rotundus on isoprenaline-induced myocardial infarction. Thirty five Wistar rats, aged 60-100 days with body wt. 150-200 g, pretreated with ethanolic extract of Cyperus rotundus L. (@ 250 and 500 mg/kg body wt.) orally before induction of myocardial necrosis by administrating isoprenaline (85 mg/kg, s.c.) on 19th and 20th day of the pretreatment period. The treated rats were examined for gross functioning of heart, heart weight/body wt. Ratio, and also observed histopathologically. Further, activities of various cardiac enzymes such as aspartate transaminase, alanine transaminase, creatinine kinase-myoglobulin, lactate dehydrogenase, and the gold marker troponin-I were also determined. The levels altered by isoproterenol were found to be restored significantly by the test extracts especially at higher dose. Biochemical observations viz., serum ALT (P<0.0001), AST (P<0.0001), creatine kinase-myoglobulin (CK-MB) (P<0.0001), LDH (P<0.0001) demonstrated significant cardioprotective activity of the ethanolic extract of C. rotundus(500 mg/kg body wt.), against isoprenaline induced myocardial infarction. These results were also substantiated by physical parameters and histopathological observations. All these results were comparable with that of two standard drugs metoprolol (10 mg/kg/day), ramipril (3 mg/kg/day) as well as polyherbal formulation Abana (50 mg/kg/day).
ABSTRACT
Dyslipidemia is related to the progression of atherosclerosis and is an important risk factor for acute coronary syndromes. Our objective was to determine the effect of rosuvastatin on myocardial necrosis in an experimental model of acute myocardial infarction (AMI). Male Wistar rats (8-10 weeks old, 250-350 g) were subjected to definitive occlusion of the left anterior descending coronary artery to cause AMI. Animals were divided into 6 groups of 8 to 11 rats per group: G1, normocholesterolemic diet; G2, normocholesterolemic diet and rosuvastatin (1 mg·kg-1·day-1) 30 days after AMI; G3, normocholesterolemic diet and rosuvastatin (1 mg·kg-1·day-1) 30 days before and after AMI; G4, hypercholesterolemic diet; G5, hypercholesterolemic diet and rosuvastatin (1 mg·kg-1·day-1) 30 days after AMI; G6, hypercholesterolemic diet and rosuvastatin (1 mg·kg-1·day-1) 30 days before and after AMI. Left ventricular function was determined by echocardiography and percent infarct area by histology. Fractional shortening of the left ventricle was normal at baseline and decreased significantly after AMI (P < 0.05 in all groups), being lower in G4 and G5 than in the other groups. No significant difference in fractional shortening was observed between G6 and the groups on the normocholesterolemic diet. Percent infarct area was significantly higher in G4 than in G3. No significant differences were observed in infarct area among the other groups. We conclude that a hypercholesterolemic diet resulted in reduced cardiac function after AMI, which was reversed with rosuvastatin when started 30 days before AMI. A normocholesterolemic diet associated with rosuvastatin before and after AMI prevented myocardial necrosis when compared with the hypercholesterolemic condition.
Subject(s)
Animals , Male , Rats , Fluorobenzenes/therapeutic use , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Myocardial Infarction/pathology , Myocardium/pathology , Pyrimidines/therapeutic use , Sulfonamides/therapeutic use , Cholesterol, Dietary/adverse effects , Disease Models, Animal , Echocardiography , Hypercholesterolemia/complications , Hypercholesterolemia/drug therapy , Myocardial Infarction/etiology , Necrosis/prevention & control , Rats, WistarABSTRACT
Objective To investigate the effect of tirofiban on myocardial necrosis biomarker after percutaneous coronary interventions(PCI)in patients with aspirin resistance(AR).Methods 374 consecutive patients with aspirin 100 mg≥1 week,receiving no other antiplatelet therapy,scheduled for PCI were enrolled.all patients were given an loading dose of 300 mg clopidogrel at least 12 hours before PCI and an 75 mg maintenance dose per day.Patients were randomized into tirofiban group(n=38)and control group(n=45)after PCI.The levels of CKMB,TnI at 8,12,and 24 hours after PCI were measured in all patients;if the CK-MB,TnI value was above normal upper limitation,it was considered elevated.Results 83 patients were AR(22.2%)and 54.2%of them are females.The frequencies of CK-MB elevation were 15(39.5%)in tirofiban group and 19(42.2%)in control group,and TnI elevation was 18(47.4%)and 23(51.1%)in the two groups respectively.Conclusion Tirofiban can not decrease the elevation level of CK-MB and TnI in patients with AR after PCI.
ABSTRACT
Cardio-protective action of synthetic peptide 6A, fibrinogen degradation segment, was observed on the myocardial injury model produced by subcutaneous injection of iso-proterenol (30 mg?kg-1-d-1) into rat. Treatment with peptide 6A (50 ?mol?kg-1? d-1,iv) significantly ameliorated isoproterenol-induced myocardial lesion, inhibited release of myocardial creatine phosphokinase, ?-hydroxybutyratedehydrogenase, lactate dehydrogenase and gluta-mate-oxaloacetate transaminase, lowered plasma fibrinogen content,and markedly prevented myocardial calcium accumulation. The results suggest that peptide 6A could have potential significance for clinical therapy of ischemia heart diseases.